Role of cytokines and oxidative stress in the formation of gastric hemorrhagic ulcer in diabetes rats---protective effects of pentoxifylline and lysozyme chloride

碩士 === 國立成功大學 === 藥理學研究所 === 98 === Background: Diabetes mellitus(DM) is a world widespread disease. This fatal disease can provoke oxidative stress and result in organ dysfunction. Cytokine, including tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β), are pro-inflammatory substances that m...

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Bibliographic Details
Main Authors: En-NungChou, 周恩儂
Other Authors: Chen-Road Hung
Format: Others
Language:zh-TW
Published: 2010
Online Access:http://ndltd.ncl.edu.tw/handle/31968036087523839013
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Summary:碩士 === 國立成功大學 === 藥理學研究所 === 98 === Background: Diabetes mellitus(DM) is a world widespread disease. This fatal disease can provoke oxidative stress and result in organ dysfunction. Cytokine, including tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β), are pro-inflammatory substances that may involve in the etiology of DM formation. Gastric damage is one of important manifestations in DM disease nevertheless, documents concerning with the influence of cytokines and oxidative stress in the formation of gastric hemorrhagic ulcer is lacking. Purpose: The aim of the present study is thus to investigate the role of cytokines and oxidative stress in the formation of gastric hemorrhage and ulcer in DM rats. Additionally, cytoprotective effects of pentoxifylline (PTX) and lysozyme chloride (LYZ) on gastric damage in DM rats were studied. Results: The results showed that the expression of TNF-α or IL-1β was increased in streptozotocin (STZ)-induced DM rat gastric mucosa. Moreover, high relationship of TNF-α and IL-1β generation to gastric hemorrhagic ulcer were found in those DM rats. This hemorrhagic ulcer and various ulcerogenic parameters were dose-dependently attenuated by daily intragastric PTX and LYZ although blood glucose was not affected. Insulin decreased gastric ulcer, mucosal lipid peroxides and histamine levels while mucosal glutathione concentration was elevated. Conclusion: DM could produce gastric hemorrhagic ulcer via aggravation of gastric acid back-diffusion, LPO generation, histamine production and pro-inflammation cytokines such as TNF-α and IL-1β release that could be ameliorated by PTX , LYZ and insulin in rats.